Obstructive sleep apnea (OSA) is defined as recurrent cessation of breathing with upper airway obstruction occurring during sleep, resulting in substantially reduced (hypopnea) or complete cessation (apnea) of airflow despite ongoing breathing efforts. By convention, the patient must experience more than 30 episodes lasting more than 10 seconds or more than five abnormal breathing disturbances (hypopneas or apneas) per hour of sleep. In most cases the person is unaware that a disturbance is taking place. Referring now to FIG. 1, the human upper airway anatomy consists of the mandible bone 12, tongue 2, pharynx 3, hyoid bone 4, palate 5, uvula 6, epiglottis 7, lips 8, larynx 9, geniohyoid 10, mylohyoid 11, and adjacent facial structures. This anatomy plays a central role in speaking, breathing, mastication and swallowing. The airway is composed of numerous muscles and soft tissue but lacks rigid or bony support. Most notably, it contains a collapsible portion that extends from the hard palate 5 to the larynx 9. Although the ability of the upper airway to change shape and momentarily close is essential for speech and swallowing during an awake state, this feature also provides the opportunity for collapse at inopportune times such as during sleep. Although non-obese individuals may suffer from OSA, obesity is the main epidemiologic risk factor. It can influence both the structure1 and function2 of skeletal muscles. The interplay and correlated movements between all the anatomical structures is complex. These various physiological traits and the potential for each to influence sleep apnea pathophysiology have been described in detail in review articles3. The pathophysiological causes of OSA likely vary considerably between individuals. Important components likely include upper airway anatomy, the ability of the upper airway dilator muscles to respond to respiratory challenge during sleep, the propensity to wake from increased respiratory drive during sleep (arousal threshold), the stability of the respiratory control system (loop gain), and the potential for state-related changes in lung volume to influence these factors. Ultimately, the maintenance of pharyngeal patency depends on the equilibrium between occluding and dilating forces4. Upper airway dilator muscle activity is crucial to the counteraction of the negative intraluminal pressure generated in the pharynx during inspiration. Diminution of this activity during sleep is thought to play a central role in pharyngeal collapse and obstruction in patients with OSA.5 1 Wade et al. (1990)2 Schwartz et al. (1998)3 White (2005)(2006), Schwab (1995)4 Douglas et al. (1994), Young et al. (1993)5 Remmers et al. (1978), Block et al. (1984) White (2006), Guilleminault et al. (1976)
The development of occlusion in this disorder has been related to “prolapsed” of the tongue into the pharynx. The tongue being prolapsed has been attributed to diminished neuromuscular activity in the genioglossus muscle inside the tongue which protrudes it forward, when it is activated.6 Activation of the genioglossus (GG), the main tongue protrudor, has been shown to reduce pharyngeal resistance and collapsibility by far more than all other upper airway dilators. 6 Remmers et al
There are a variety of treatments for OSA, but continuous positive airway pressure (CPAP), in which a nose mask is attached via a tube to a machine to blow pressurized air into the pharynx and push the collapsed section open, is still the gold standard in the treatment. Surgical procedures aiming for tissue reduction or stiffening to widen the pharynx have proven to be unreliable or to have adverse effects. However, as most patients dislike or refuse to use a mask for CPAP treatment, a new procedure involving implants are needed. Multiple trials attempting to relieve OSA by functional electric stimulation of upper airway dilators during sleep resulted in modest and/or inconsistent results.7 Numerous attempts have been made towards treating OSA by placing implants into the tongue and are known in prior art, for example, the Pavad Medical tongue stabilization device U.S. Pat. Nos. 7,909,037 and 7,909,038, both dated Mar. 22, 2011. Another implant for treating OSA of is the Restore Medical implant disclosed in U.S. Pat. No. 7,401,611 dated Jul. 22, 2008, or the Revent Medical implant disclosed in U.S. Pat. No. 8,167,787 dated May 1, 2012 and U.S. Pat. No. 8,327,854 dated Dec. 11, 2012. All of the mentioned patents involve surgical procedures, which may not be suitable for some patients and/or which are extremely time consuming for inserting. 7Edmonds et al. (1992), Miki et al. (1989), Decker et al. (1993), Eisele et al. (1997), Guilleminault et al. (1995), Schnall et al. (1995), Schwartz et al. (1996), Oliven et al. (2001, 2003, 2007), Eastwood et al. (2003)
What is needed therefore is a surgically fast and minimally invasive tongue implant to treat OSA, which can deform like the tongue to comply with physiological tasks, but changing its rigidity to reliably and safely open up the pharyngeal airway blocked by the tongue by deforming it and providing a torque. The implant should stiffen the tongue along the base of the tongue and protrude it. Furthermore, it must minimize relative movement between implanted member and surface area in contact with the tongue to avoid abrasion of the implant.